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Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.
The patient was extubated on Day-3 of the hospital stay. The patient improved, and on Day-11 of the hospital stay — he was off inotropes and on a small dose of a ß-blocker. There is no definite evidence of acute ischemia. (ie, Some residual ischemia in the infarct border might still be present.
Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. There’s competing sinus bradycardia and junctional rhythm, with otherwise normal conduction, borderline right axis, normal R wave progression and voltages. What do you think?
A few days into her hospital stay she developed chest discomfort and the following ECG was recorded. The ECG below was on file and was taken a few days earlier, on the day of admission to the hospital. Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation. What do you think?
A prior ECG was available for comparison: Normal One might be tempted to interpret the ST depression as ischemia, but as Smith says, "when the QT is impossibly long, think of hypokalemia and a U-wave rather than T-wave." The patient was admitted to the ICU for close monitoring and electrolyte repletion and had an uneventful hospital course.
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization. Chest trauma was suspected on initial exam. See this case , this case , and this case.
I see the following: The rhythm is sinus bradycardia at ~55-60/minute. About 20 minutes later ( on the way to the hospital ) — the patient's CP resolved, and ECG #1 was recorded. ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
That said — obvious findings include: i ) Marked bradycardia! — My Immediate Impression — was that this elderly woman with a several week history of symptoms would most likely leave the hospital with a pacemaker. This suggests ischemia of uncertain duration. be regular! —
There are 3 etiologies I always think of with bradycardia and AV block: 1. There was no evidence of ischemia. In addition to ruling out rate-slowing medication serum electrolyte disorders and/or ischemia/infarction as potential causes of bradyarrhythmias one should also rule out hypothyroidism + sleep apnea. Hyperkalemia.
Patients use them to observe their heart activity by themselves when they are not in the hospital. Though their accuracy is not as high as a hospital ECG machine, they are very beneficial in detecting problems in any medical emergency and providing information about long-term heart activity.
A few days later an ECG was repeated which showed normal sinus rhythm with no further hyperkalemia findings: After a 3-week hospitalization for acute renal failure, hyperkalemia, and compartment syndrome, the patient was discharged to acute rehab. He went emergently to the OR for fasciotomy due to compartment syndrome. With a twist.
Whether these EKGs show myocarditis, a normal variant, or something else, they are overall not typical of transmural ischemia of the anterior or high lateral walls. Patient 1 remained in the hospital overnight. He had multiple episodes of bradycardia and nonsustained ventricular tachycardia.
After the heart rate increased slightly, here was the repeat ECG: Sinus bradycardia, only slightly faster rate than prior. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI.
There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still. The corrected QT interval is extremely long, about 500 ms. However, the mean level (2.50.4
Such findings would normally suggest primary ischemia with concomitant surveillance of coronary occlusion, but these ST/T changes might very well be secondary to the Escape mechanism at hand. Hospital transport was unremarkable. The patient advised overall improvement with complete resolution of symptoms.
Case 4 Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 Patient presentation is important This was a 60-something with acute chest pain: There is sinus bradycardia at a rate of 44. In case you were wondering about the T-waves and bradycardia, the K was normal. Why bradycardia?
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). 121.022866.
Evidence of acute ischemia (may be subtle) vii. PVCs N ot generally considered abnormal ECG findings: Isolated PAC, First Degree AV Block, Sinus bradycardia at a rate of 35-45, and Nonspecific ST-T abnormalities (even if different from a previous ECG). Left BBB vi. Pathologic Q-waves viii. LVH or RV d. Abnormal but less worrisome: i.
Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI. 7 steps to missing posterior Occlusion MI, and how to avoid them Interventionalist at the Receiving Hospital: "No STEMI, no cath.
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